The Post-modern Retrovirus
Part 2

2,468 words

The inability to develop a diagnostic test of scientific rigor is a consequence of the inability to isolate or purify the virus. Instead, what was done by HIV pioneers was the stimulation of cell culture samples with hormones, mitogens and oxidase in order to get the abnormal proteins said to be HIV specific. Virologist Stefan Lanka claims that there is no evidence for the virus even existing, arguing that placing cells from HIV negative persons under the same stressful conditions yields the same protein reactions. Such controls are absent in AIDS literature.[1]

Manufacturers of testing kits are admittedly honest about the limitations of their products. Accompanying all kits are clear disclaimers warning against use for screening or confirmation of AIDS. Ironically, some of the prominent test designers have voiced views on HIV/AIDS that are quite contrary to the industry that harnessed their technical expertise. Pivotal developer of the ELISA test, Rodney Richards, is an HIV dissident; as is the inventor of PCR, Kary Mullis.

Testing played an important role in engineering the AIDS phenomenon. The apparent rise of HIV from 1990 to 2000, constituting an epidemic, was really only a function of the epidemic of testing. Testing epidemics began in the United States and soon infected all countries that accepted the new HIV/AIDS hypothesis. But after just a few years of testing, the prevalence in each country would flatline, which is inconsistent with a viral epidemic but consistent with a retrovirus that was long established in the population.[2]

For a small cost, the tests offer an unparalleled return on investment for the industry as a whole, as a positive diagnosis typically results in patient medication. Notwithstanding the long dormancy and total lack of symptoms, the patients commence treatment when they would be otherwise oblivious for up to 20 years. Promises of slowing down disease progression and even reducing communicability[3] are just some of the selling points for an industry that has failed to deliver a universal cure or vaccine. Unfortunately for those freshly diagnosed, it is the overriding sense of civic duty, naïve trust in authority and generous subsidies that encourage long-term commitment to drug treatment that they have little understanding of. The reciprocation of this trust has been gross pharmacological malpractice.

When the pioneering drug azidothymidine (AZT) was released onto the market, few were aware that it was an old drug for a new disease. Originally designed to treat cancer but shelved because it was deemed too toxic, the AIDS establishment demonstrated a remarkable level of acumen by giving the drug a second life. Retroviruses are indeed considered natural carcinogens as they are not cytocidal (cell-killing), rather they are associated with abnormal cell growth like neoplasma (cancers). These symptoms, however, are not observed in AIDS patients, nor is there evidence for HIV killing or suppressing T-cells of the immune system. This lack of evidence is what led to the current supposition of AIDS establishment scientists: that HIV “primes T-cells to commit suicide at some later date.”[4] No virus kills thousands of times more cells than it infects – the modest replicator HIV being no different. In spite of this, big pharma and its governmental emissaries decided that the only thing they could do to take action was to argue that toxic drugs are necessary.

Anti-retroviral drugs are DNA chain-terminators and protease inhibitors, meaning that their actions are indiscriminate and destructive to healthy cells. This is why many studies show that patients on antiretroviral drugs are more symptomatic of AIDS-defining diseases compared to those not receiving the drugs.[5] After just three years of taking AZT, recipients suffer lymphoma at a rate of 46%, which is what led to the classification of several lymphoma types as AIDS-defining.[6] Experiments conducted on mice, dogs and monkeys have shown that anti-HIV drugs cause immunodeficiency, anemia, muscle atrophy, nephropathy, various cancers, nerve and liver damage, as well as retarded development and abortions of fetuses.[7] A study published in the Journal of AIDS found that for 104 pregnant women treated with AZT, 24 had babies with heart defects, malformed spines, extra fingers, misplaced ears, albinism or were so deformed that abortion occurred naturally or had to be “therapeutically” induced.[8]

Anti-HIV drugs can sometimes have positive effects on patients in the short term due to corollary antibacterial and antiviral properties of the medication, but the inevitable long-term effects of DNA-chain terminator drugs are dire. A study in Nature Genetics showed that anti-HIV drugs accelerate aging immensely in patients, because nucleoside analogue agents accumulate somatic mitochondrial mutations, causing multi-organ disease and senescence normally seen among the elderly.[9] The Lancet published data on 1,749 HIV-positive subjects, showing that not only did AZT fail to prevent AIDS, but mortality increased by 25%.[10]

Empirical indictments such as these were little more than background noise during the bureaucratic wave-through that escorted the early AZT trials into approval. Thanks to requests made under freedom of information acts, journalists were able to identify the fingerprints on an already smoking gun: abandoned trials, omission of data, federal agency collusion, AZT patients who were given blood transfusions, and supposed double-blind studies that were totally compromised because subjects pooled the drugs and placebos among each other.[11]

Officials now publicly acknowledge the deadly mistake that was AZT,[12] but at the time anti-AZT views were called “the realm of quackery” by the President of the American Council on Science and Health.[13] Remarkably, anti-HIV drugs still incorporate AZT as part of the drug cocktail called combination therapy and are trumpeted for being less toxic and less lethal than before. The problem is that the operating paradigm still takes a pharmacological sledgehammer to a peanut. Only one in 10,000 cells actively copy HIV, meaning that a huge number of cells need to be killed to inhibit the virus.[14]

Historically, AIDS medication was divided into several costly pills until 2001 when an Indian manufacturer of generic medications produced a pill that contained three retrovirals (patented by different pharmaceutical giants) of combination therapy. This was possible because India was not a signatory of the TRIPS global patent treaty. The price of HIV treatment dropped from about $10,000 a year to a little over $100 – which was a consequence of fierce competition in a country that had no patents on medicines until 2005.[15] India became known as the pharmacy of the developing world thanks to its breaking of big pharma’s monopolistic price fixing. The same medications in the First World remain very expensive, but it is these drugs that are designated for Third World aid via Western partnerships.

In 2015, the BBC enthusiastically reported on the new campaign to get all gay men to start taking daily medication that could somehow prevent gay men from contracting HIV.[16] Researchers compared it to the pill for women, and Britain’s NHS was considering how to adopt the drugs at a proposed cost to taxpayers of £4320 per patient annually. In Africa, wealthier countries like Botswana and South Africa with their well-established AIDS infrastructure suffer rates that are among the worst on the continent. Interestingly, in neighboring Zimbabwe rates plummeted as the economy collapsed – with the official explanation being that lower living standards meant fewer affairs and less promiscuity.[17]

With so much money pumped into the AIDS-industrial complex, it’s accurate to say that the science took a passenger seat while corporate values, image and PR drove the enterprise forward. In fact, the very image of HIV that is strewn across posters and textbooks is disputed as a potential case of mistaken identity. Pathologist and electron microscopist Étienne de Harven was the first person to produce an image of a retrovirus using electron microscopy, however he vehemently denies that the iconic images purported to be HIV are identified correctly, instead pointing to innocuous human endogenous viruses (HERVs) related to the host’s own genome – emitted when scientists add the growth factors and hormones.[18]

Ironically, there are some elements of official AIDS science that, while not disputed, are passively suppressed. One of these is the transmissibility of HIV. Coitus with an HIV-positive person carries a contraction risk of about 1 in 1000.[19] Like all viruses, HIV depends primarily upon perinatal (mother to child) transmission for its continued existence. This mode of infection is about 50% efficient, or roughly 500 times more efficient than sexual transmission.[20] The reason that this information is not presented to the public is because it conflicts with the narrative of HIV as a contagious sexual epidemic. Of the many millions of perinatally infected HIV-positives, the vast majority remain healthy and without AIDS progression as young adults. Every year the US Army tests all of its new applicants, including young adults, and in the process identifies thousands of completely healthy people who are HIV-positive. It can be inferred that these young and healthy adults were infected at pregnancy 16 to 20 years prior to their enlisting in the army. This phenomenon of healthy young people who have carried the virus since they were a fetus is consistent with the global population of millions who are long-term carriers and healthy.[21]

As far as improbable epidemiology goes, perhaps none is more remarkable than the record of virtually no doctor or researcher of HIV ever developing AIDS as a result of accidental HIV contraction. For perspective, thousands of doctors pick up hepatitis from their patients every year due to clinical mishaps. Other epidemiological blind spots that contravene the orthodox predictions include the lack of an epidemic among sex workers or a crossover into the mainstream heterosexual population.

Biological mathematician Rebecca Culshaw documented another dozen predictions of the HIV establishment that failed to transpire, the most famous of which was the announcement that a vaccine would be available by 1987.[22] In any case, the long wait for the phantom vaccine and promised heterosexual epidemic never deflated the enthusiasm of HIV industry flag bearers. Adherence to HIV creed remains religiously institutionalized even though the elite criteria for this viral Messiah remains wholly unfulfilled. Duesberg and Ellison explain:[23]

1. No virus has been scientifically shown to cause disease only after being neutralized by antibodies
2. No virus has been proven to cause disease after long latent periods rather than upon initial infection
3. No virus has been shown to kill thousands of cells more than it infects
4. No retrovirus, including HIV, has ever been demonstrated to systematically kill any of the cells it infects
5. No virus has been found that causes radically different diseases in different hosts, including illnesses not caused by immune suppression
6. No sexually transmitted disease has remained so rigidly confined to specific risk groups (to males for 10 full years)

Their conclusion is that HIV/AIDS currently fails to meet the conditions of an epidemic as it is neither spreading nor active. What the data ardently suggest is that HIV is insufficient and unnecessary to cause disease; it is a passenger virus.[24] Passenger viruses can be associated with healthy people as well as sufferers of virus-independent diseases. There are multiple instances of passenger viruses in the human population: adenovirus, cytomegalovirus and reovirus.[25]

The mythical provenance of HIV in the jungles of Africa is an unnecessarily obscure and improbable origin story. Consumption of bushmeat has been going on for millennia, so to learn that the AIDS virus surreptitiously delayed its zoonosis until the 20^th century is particularly beguiling. This officially occurred not once but twice, in the same time period, in separate parts of Africa, from different species of monkey. The claim of two types of HIV arose as a way to explain the radically inconsistent epidemiology. The ancestor virus of HIV-1 allegedly transferred from monkeys to humans in Cameroon around 1930,[26] while the zoonosis of HIV-2 allegedly occurred around 1940 in Guinea-Bissau.[27]

Official AIDS science argues that an immigrant from Haiti brought HIV to America in the late 1960s. This timeframe suits the narrative of AIDS progression being 10-15 years, which lands in the early 1980s epidemic. While the culture of promiscuity was no greater than in prior decades, there was a notable change in drug culture, which was a global phenomenon. In America, the home drug lab revolution synthesized substances more potent than ever and streamlined accessibility and affordability to suburbanites.

Notes

[1] Interview with Dr Stefan Lanka. Conducted by Huw Christie Williams. London, 1994

[2] Duesberg, P. H. AIDS acquired by drug consumption and other noncontagious risk factors. Pharmacol. Ther. 55: 201-277

[3] The treatment that allows HIV-positive gay men to have unprotected sex: 8-year study reveals those on drugs to combat the killer virus are non-infectious. By Stephen Matthews. 25 July 2018. Daily Mail

[4] Culshaw, R. Science Sold Out: Does HIV Really Cause AIDS? Page 73. Berkeley, CA: North

Atlantic Books (2007)

[5] Bauer, H. The Origin, Persistence and Failings of HIV/AIDS Theory. Jefferson, NC: McFarland & Company, Inc., Publishers (2007)

[6] Pluda, J.M. et al. Development of non-Hodgkin lymphoma in a cohort of patients with severe human immunodeficiency virus (HIV) infection on long-term antiretroviral therapy. Ann Intern Med., 113(4): 276-82

[7] Duesberg, P., Koehnlein, C., Rasnick, D. The chemical bases of the various AIDS epidemics: recreational drugs, anti-viral chemotherapy and malnutrition. J. Biosci. 28: 383-412

[8] Kumar, R.M., Hughes, P.F., Khurranna, A. Zidovudine Use in Pregnancy: A Report on 104 Cases and the Occurrence of Birth Defects. Journal of Acquired Immune Deficiency Syndromes, 7(10): 1034

[9] Payne, B.A., Wilson, I.J., Hateley, C.A., Horvath, R., Santibanez-Koref, M., Samuels, D.C., Price, D.A., Chinnery, P.F. Mitochondrial aging is accelerated by anti-retroviral therapy through the clonal expansion of mtDNA mutations. Nat. Genet. 43: 806-810

[10] Seligmann, M., Warrell, D.A., Aboulker J-P., et al. Concorde: MRC/ANRS randomised double-blind controlled trial of immediate and deferred zidovudine in symptom-free HIV infection. Lancet, 343: 871-881

[11] AZT on trial. By John Lauritsen. 19 October 1987. New York Native

[12] The AIDS Industry. 21 July 2010. CrossTalk with Peter Lavelle. RT

[13] Whelan, E.M. Fringe of Science. Letter in response to Duesberg & Ellison article in Policy Review Dec 1990

[14] Sins Of Omission: The AZT Scandal. By Celia Farber. November 1989. Spin

[15] Cheap generic drugs from India turned the tide against HIV and this court case means this can continue. By Unni Karunakara. 1 April 2013. The Independent

[16] Give HIV drugs to healthy gay men. By James Gallagher. 24 February 2015. BBC

[17] In Zimbabwe, Fewer Affairs And Less HIV. By Craig Timberg. 13 July 2007. The Washington Post

[18] De Harven, E., Roussez, J. 2008. Ten Lies about AIDS. Bloomington, IN: Trafford Publishing

[19] Blattner, W. A. 1991. HIV epidemiology: past, present, and future. FASEB J 5: 2340-2348

[20] Duesberg, P. H. 1992. AIDS Acquired by Drug Consumption and Other Noncontagious Risk Factors. Pharmacology & Therapeutics, 55: 201–277

[21] Duesberg, P. H. 1998, 2^nd Ed. Inventing the AIDS Virus (p185). Washington, DC: Regnery Publishing

[22] Culshaw, R. 2007. Science Sold Out: Does HIV Really Cause AIDS? Appendix A: Failed Predictions of the HIV Hypothesis. Berkeley, CA: North Atlantic Books

[23] Is HIV cause of AIDS? Peter H. Duesberg and Brian J. Ellison respond to their critics. Policy Review Dec. 1990

[24] Duesberg, P. (1994) Infectious AIDS–stretching the germ theory beyond its limits. Int. Arch. Allergy Immunol. 103: 118-127

[25] Fields, B. (2001) Field’s Virology. Lippincott Williams & Wilkins, Philadelphia

[26] Korber, B. et al. 2000. Timing the Ancestor of the HIV-1 Pandemic Strains. Science, 288: 1789-96

[27] Lemey, P., Pybus, O. G., Wang, B., et al. Tracing the origin and history of the HIV-2 epidemic. Proceedings of the National Academy of Sciences of the United States of America, 100(11): 6588–6592